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J Biol Chem, Vol. 275, Issue 7, 4592-4598, February 18, 2000
From the Trypsin is widely expressed in various
non-pancreatic tissues at low levels and overexpressed in some types of
human cancers. In the present study, we found that trypsin stimulates
integrin-dependent adhesion and growth of MKN-1 human
gastric carcinoma cells. MKN-1 cells expressed both
proteinase-activated receptor-1 (PAR-1) and PAR-2, which are activated
by thrombin and trypsin, respectively. Both trypsin and the PAR-2
ligand SLIGKV promoted integrin
Trypsin Stimulates Integrin
5
1-dependent Adhesion to
Fibronectin and Proliferation of Human Gastric Carcinoma Cells
through Activation of Proteinase-activated Receptor-2*
§,,§, and§¶
Division of Cell Biology, Kihara Institute
for Biological Research, and § Graduate School of Integrated
Science, Yokohama City University, 641-12 Maioka-cho, Totsuka-ku,
Yokohama 244-0813, Japan
5
1-mediated adhesion of MKN-1 cells
to fibronectin, and less effectively integrin v3-mediated cell adhesion to vitronectin,
but not that to type IV collagen or laminin-1 at all. Thrombin and the
PAR-1 ligand SFLLRN promoted the cell adhesion to vitronectin more
strongly than trypsin or the PAR-2 ligand, but not the cell adhesion to fibronectin at all. The cell adhesion-stimulating effect of the PAR-2
ligand was significantly reduced by the pre-treatment of cells with
trypsin, indicating that the effect of trypsin is mediated by PAR-2
activation. The trypsin-stimulated cell adhesion to vitronectin, but
not to fibronectin, was effectively inhibited by the Gi
protein blocker pertussis toxin, and both cell adhesions were
completely inhibited by the Src kinase inhibitor herbimycin A. Furthermore, trypsin and the PAR-2 ligand stimulated growth of MKN-1
cells more strongly than thrombin or the PAR-1 ligand. These results show that trypsin regulates cellular adhesion and proliferation by
inducing PAR-2/G protein signalings, and that the integrin 51- and integrin
v3-dependent cell adhesions
are regulated by different PAR/G protein signalings.
*
This work was supported by grants-in-aid from the Ryoichi
Naito Foundation for Medical Research and from the Ministry of
Education, Culture, Sports and Science of Japan.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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